OBJECTIVES: To determine whether endotoxic shock decreases the renal gluconeogenic capacity and the renal artery blood flow. METHODS: An in-vivo, murine, nonrecirculating kidney perfusion model was studied in a trauma research laboratory. Each of 12 fasted, male Holtzman rats (shock n = 6, control n = 6) was injected with 1 mL of normal saline or endotoxin (20 mg/kg). Five hours after the injection, all the rats were anesthetized and blood samples were obtained for the determination of the plasma glucose. Right renal artery blood flow was measured by an ultrasonic small-animal flow meter. The kidney was then perfused via the renal artery with 37 degrees C, oxygenated, glucose-free Krebs-Henseleit solution in the presence of 100 mumol of phloridzin to inhibit the cellular uptake of glucose. Renal glucose production was determined by measuring glucose in both renal vein effluent and urine. After 30 minutes of equilibration, 5 mmol of lactate and 0.5 mmol of pyruvate were added to the perfusate as a gluconeogenic substrate. Renal vein and ureteral effluent samples were collected after 5, 10, and 15 minutes. RESULTS: The endotoxic shock group showed hypoglycemia (p < 0.05) as well as a decrease in renal artery blood flow (p < 0.05). Gluconeogenic stimulation was demonstrable in both the control and the endotoxic shock groups after 15 minutes of perfusion with substrate (p < 0.05). However, renal gluconeogenesis was significantly attenuated in the endotoxic shock group compared with the control. CONCLUSIONS: Renal glucose production in response to a gluconeogenic substrate is significantly attenuated during the hypoglycemic phase of endotoxic shock. Endotoxic shock also causes a significant decrease of renal artery blood flow.
OBJECTIVES: To determine whether endotoxic shock decreases the renal gluconeogenic capacity and the renal artery blood flow. METHODS: An in-vivo, murine, nonrecirculating kidney perfusion model was studied in a trauma research laboratory. Each of 12 fasted, male Holtzman rats (shock n = 6, control n = 6) was injected with 1 mL of normal saline or endotoxin (20 mg/kg). Five hours after the injection, all the rats were anesthetized and blood samples were obtained for the determination of the plasma glucose. Right renal artery blood flow was measured by an ultrasonic small-animal flow meter. The kidney was then perfused via the renal artery with 37 degrees C, oxygenated, glucose-free Krebs-Henseleit solution in the presence of 100 mumol of phloridzin to inhibit the cellular uptake of glucose. Renal glucose production was determined by measuring glucose in both renal vein effluent and urine. After 30 minutes of equilibration, 5 mmol of lactate and 0.5 mmol of pyruvate were added to the perfusate as a gluconeogenic substrate. Renal vein and ureteral effluent samples were collected after 5, 10, and 15 minutes. RESULTS: The endotoxic shock group showed hypoglycemia (p < 0.05) as well as a decrease in renal artery blood flow (p < 0.05). Gluconeogenic stimulation was demonstrable in both the control and the endotoxic shock groups after 15 minutes of perfusion with substrate (p < 0.05). However, renal gluconeogenesis was significantly attenuated in the endotoxic shock group compared with the control. CONCLUSIONS:Renal glucose production in response to a gluconeogenic substrate is significantly attenuated during the hypoglycemic phase of endotoxic shock. Endotoxic shock also causes a significant decrease of renal artery blood flow.
Authors: Michael Gröger; Melanie Hogg; Essam Abdelsalam; Sandra Kress; Andrea Hoffmann; Bettina Stahl; Enrico Calzia; Ulrich Wachter; Josef A Vogt; Rui Wang; Tamara Merz; Peter Radermacher; Oscar McCook Journal: Front Med (Lausanne) Date: 2022-04-29